Helicobacter pylori (H. pylon) is closely related to the pathogenesis of chronic gastritis, peptic ulcer disease, gastric carcinoma, and gastric MALT-lymphoma. However, the mechanisms of H. Pylon-induced gastric mucosal damage and carcinogenesis have not been fully understood. We investigated the effects of H. pylon infection and H. Pylon-induced gastric inflammation on the gene expression of gastric epithelial cells. Because reactive oxygen intermediates (ROI) are increased in the H. pyloni-infected gastric mucosa and ROI may be important in inducing gastric mucosal damage, we examined the gene expression profile of gastric epithelial cells in response to oxidative stress. We found that oxidative stress activates the transcription factors, NF-κB and AP-1, and upregulates the expression of interleukin-8 and cyclooxygenase-2. The expression of several genes involving cell cycle regulation, apoptosis, and MAP kinase pathways were also found to be affected by oxidative stress. These results suggest that, in H. pylon-infected gastric mucosa, prolonged inflammatory condition alters the gene expression patterns of gastric epithelial cells which may be related to the gastric carcinogenesis.